Mechanistically, RBP-J deficiency in myeloid cells impeded the differentiation of moTAMs, but promoted the proliferation and pro-tumor cytokine [e.g., interleukin 10 (IL-10)] production of kclTAMs by upregulating WNT-β-CATENIN signaling, and then accelerating the progression of murine orthotopic HCC [91]. This evidence concerns the gene RBPJ and hepatocellular carcinoma.